Placental Dysfunction in Suramin-Treated Rats: Impact of Maternal Diabetes and Effects of Antioxidative Treatment

Nash, Peppi; Olovsson, Matts; Eriksson, Ulf J.

doi:10.1016/j.jsgi.2004.12.002

Cited by 15 publications

(8 citation statements)

References 58 publications

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“…This presumption finds support in the similarity of placental data obtained in suramin-treated and FRD dams. Indeed, it has been showed that suramin treatment in dams drastically reduced placental and renal blood vessel areas, being these parameters indicative for the hypertensive state developed by these dams [34]. Interestingly, and in accordance with its improving effect on glucose homeostasis, metformin treatment in FRD dams fully prevented placental dysfunction.…”

Section: Discussionmentioning

confidence: 88%

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

et al. 2012

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The intake of a fructose-rich diet (FRD) in the normal female rat induces features similar to those observed in the human metabolic syndrome phenotype. We studied the impact of FRD administration to mothers on pregnancy outcome. On gestational day (Gd) zero rats were assigned to either group: ad libitum drinking tap water alone (normal diet, ND) or containing fructose (10% w/vol; FRD) through pregnancy; all rats were fed a Purina chow diet ad libitum ND and FRD rats were daily cotreated or not with metformin (60 mg/Kg/day oral; ND + MF and FRD + MF) and submitted to a high glucose load test on Gd 14. Additionally, placentas from different groups were studied on Gd 20. Data indicated that: (1) although FRD rats well tolerated glucose overload, their circulating levels of insulin were significantly higher than in ND rats; (2) the mesometrial triangle blood vessel area was significantly lower in placentas from FRD than ND dams; (3) the detrimental effects of FRD administration to mothers were ameliorated by metformin cotreatment. Our study suggests that excessive intake of fructose during pregnancy enhanced the risk for developing gestational diabetes and subsequent preeclampsia, and that metformin prevented the poor pregnancy outcome induced by FRD.

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Section: Discussionmentioning

confidence: 88%

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

et al. 2012

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“…Estimations of 8-iso-PGF2␣ in fetal liver and maternal serum were performed largely in accordance with the instructions from the manufacturer (Cayman Chemical, Ann Arbor, MI), as described in previous work (31,50). The protein content of the liver samples was estimated by the method of Lowry et al (26), using bovine serum albumin as standard.…”

Section: ϫ⌬(Cp)mentioning

confidence: 99%

Genetic and environmental influence on diabetic rat embryopathy

Ejdesjö

Wentzel

Eriksson

2011

American Journal of Physiology-Endocrinology and Metabolism

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Ejdesjö A, Wentzel P, Eriksson UJ. Genetic and environmental influence on diabetic rat embryopathy. Am J Physiol Endocrinol Metab 300: E454 -E467, 2011. First published November 30, 2010 doi:10.1152/ajpendo.00543.2010We assessed genetic and environmental influence on fetal outcome in diabetic rat pregnancy. Crossing normal (N) and manifestly diabetic (MD) Wistar Furth (W) and Sprague-Dawley (L) females with W or L males yielded four different fetal genotypes (WW, LL, WL, and LW) in N or MD rat pregnancies for studies. We also evaluated fetal outcome in litters with enhanced or diminished severity of maternal MD state, denoted MD ϩ WL and MD Ϫ LW. The MDWW litters had less malformations and resorptions (0 and 19%) than the MDLL litters (17 and 30%). The MDWL litters (0 and 8%) were less maldeveloped than the MDLW litters (9 and 22%), whereas the MD ϩ WL (3 and 23%) and MD Ϫ LW (1 and 17%) litters showed increased and decreased dysmorphogenesis (compared with MDWL and MDLW litters). The pregnant MDW rats had lower serum levels of glucose, fructosamine, and branched-chain amino acids than the pregnant MDL rats, whereas the pregnant MD ϩ W and MD Ϫ L rats had levels comparable with those of the MDL and MDW rats, respectively. The 8-iso-PGF2␣ levels of the malformed MDLW offspring were increased compared with the nonmalformed MDLW offspring. Diabetes decreased fetal heart Ret and increased Bmp-4 gene expression in the MDLW offspring and caused decreased GDNF and Shh expression in the malformed fetal mandible of the MDLW offspring. We conclude that the fetal genome controls the embryonic dysmorphogenesis in diabetic pregnancy by instigating a threshold level for the teratological insult and that the maternal genome controls the teratogenic insult by (dys)regulating the maternal metabolism. diabetes in pregnancy; congenital abnormalities; teratology; animal experimentation; aldose reductase; glyceraldehyde-3-phosphate dehydrogenase; sonic hedgehog homolog; ret proto-oncogene; glial-derived neurotrophic factor; antioxidative enzymes THE INCIDENCE OF CARDIOVASCULAR, skeletal, urinary, gastrointestinal, and caudal dysgenesis-related defects is higher in offspring of women with preexisting diabetes compared with infants of nondiabetic women (4,18,27,38). Despite extensive research and optimized clinical care, diabetic embryopathy has remained etiologically enigmatic and difficult to prevent (40). The diabetes-induced alterations in embryonic development are similar to changes caused by several other teratogens, suggesting that the mechanism of diabetic dysmorphogenesis is multifactorial.The maternal environment and the fetal-maternal genotypes have been implicated in the teratogenicity of diabetic pregnancy. Thus, in diabetic women, the metabolic control (Hb A 1c levels) during the proximal part of the first trimester (29) is a strong predictor of the risk for congenital malformation (28). In experimental work, maternal metabolic deregulation has been confirmed as an important teratogenic factor (14,17,25), and a teratog...

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“…Such factors of the maternal environment include nutrient restriction (Woodall et al, 1996;Rudge et al, 1999;Redmer et al, 2004;Wu et al, 2006), oxidative stress (Maranghi et al, 1998;Nash et al, 2005;Myatt, 2006;Burdon et al, 2007), anemia (Crowe et al, 1995), hypoxia (Robinson et al, 1979(Robinson et al, , 1985Owens et al, 1987aOwens et al, , 2007Lynch and Bruce, 1989;Myatt, 2006), and hypoglycemia (Robinson et al, 1979;Lueder et al, 1992;Carver and Hay, 1995;Owens et al, 1987bOwens et al, , 2007. Nutrient restriction affects the development of the blastocyst, its implantation, and the subsequent development of the placenta (Cross and Mickelson, 2006).…”

Section: Discussionmentioning

confidence: 99%

Embryonic mortality and intrauterine growth retardation (IUGR) associated with placental alterations in pregnant rats treated with methyl methanesulfonate (MMS) at the peri-implantation stage

et al. 2008

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-Embryonic mortality and intrauterine growth retardation (IUGR) are induced by exposure of rodents to xenobiotic agents during the pregastrulation period of development. We examined the time course of the effects of methyl methanesulfonate (MMS), an alkylating agent, on conceptus development in order to clarify the relative roles of the embryo and the placenta in their induction. Pregnant rats were treated orally with a single dose of MMS (200 mg/kg) in the morning of gestation day (GD) 6 (peri-implantation stage). Embryonic mortality was increased on GD12 and thereafter by MMS treatment, with newly dead embryos showing placental hypoplasia at GD12. Embryo or fetal weight was also smaller for MMS-treated dams than for control dams from GD14 to GD20. The labyrinth zone and junctional zone (JZ) of the placenta were thinner in MMS-treated rats from GD12 to GD17 and from GD12 to GD20 (except for GD17), respectively. Furthermore, MMS-treated dams showed a smaller number of glycogen cells in the JZ on GD14. In contrast, the placental glycogen concentration was higher and the expression of glucose transporter 1 in the JZ remained at GD20. These results indicate that exposure of pregnant rats to MMS at the peri-implantation stage of embryogenesis affects placental development and growth. The placental impairment induced by MMS was likely responsible for the embryonic death observed 6 days after exposure of dams to this agent as well as for the IUGR of surviving embryos or fetuses throughout the gestation period.

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Placental Dysfunction in Suramin-Treated Rats: Impact of Maternal Diabetes and Effects of Antioxidative Treatment

Cited by 15 publications

References 58 publications

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

Genetic and environmental influence on diabetic rat embryopathy

Embryonic mortality and intrauterine growth retardation (IUGR) associated with placental alterations in pregnant rats treated with methyl methanesulfonate (MMS) at the peri-implantation stage

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